CLASS TEST - RENAL SYSTEM

ICARE MEDICAL COLLEGE

FINAL YEAR MBBS [2023]
Dr. Prithwiraj Maiti (MBBS, DNB General Medicine)
References: Harrison 21st & Brenner & Rector 11th Edition

What is acute renal failure? What are the different types? How will you manage
a case of ARF in a patient of AGE? [2+3+5]
Acute renal failure:
According to KDIGO, acute kidney injury (AKI) [previously known as acute renal
failure] is defined as any of the following:
• An increase in serum creatinine by ≥0.3 mg/dL within 48 hours
• An increase in serum creatinine to ≥1.5 times of baseline within last 7 days
• Urine output <0.5 mL/kg/hour for 6 hours.

Types of AKI:
The causes of AKI are usually divided into three pathophysiologic categories:
1. Prerenal AKI: Diseases characterized by effective hypoperfusion of the
kidneys in which there is no parenchymal damage to the kidney; it is the
most common form of AKI
2. Intrinsic AKI: Diseases involving the renal parenchyma
3. Postrenal (obstructive) AKI: Diseases associated with acute obstruction of
the urinary tract.
Common causes of AKI:
Type of AKI Common causes
Pre-renal AKI Prerenal AKI is caused by a reduction in blood
flow to the kidneys that can result from reduction in
intravascular volume. Common causes of absolute
intravascular volume depletion leading to prerenal
 AKI include:
- GI losses (e.g., diarrhea, vomiting)
- Renal losses (e.g., overdiuresis, diabetes insipidus)
- Sequestration of extracellular fluid (e.g., third spacing,
as seen in acute pancreatitis).
Intrinsic AKI Intrinsic AKI is categorized based on the anatomic
location of primary renal injury:
Location of injury Common causes
Renal vasculature Thrombosis, vasculitis, malignant
hypertension
Glomeruli Anti-GBM disease, ANCA-
associated GN, postinfectious GN,
Membranoproliferative GN, IgA-
nephropathy, SLE
Tubules Endogenous toxins, i.e. hemoglobin,
myoglobin, uric acid
Tubules + Acute allergic interstitial nephritis
Interstitium caused by NSAIDs & antibiotics
Post-renal AKI The most common causes of postrenal AKI are functional or
structural obstruction of the bladder neck due to:
- Prostatic conditions [Benign hypertrophy of prostate/
CA prostate]
- Anticholinergic agents
- Neurogenic bladder.

Management of acute renal failure in a patient with acute gastroenteritis:

Introduction:
• In acute gastroenteritis, increased frequency of loose stool results in an acute
intravascular volume depletion which is responsible for decreased renal
perfusion, causing predominantly a pre-renal type of AKI
• Along with restoration of renal perfusion by effective replacement of
intravascular fluid loss by IV fluid, increased GI loss of important
electrolytes like Na+, K+ and Mg++ should also be taken into account and
serum level of these electrolytes should be frequently monitored and should
be replaced accordingly to avoid life-threatening complications arising from
severely low level of these electrolytes
 • Last but not the least, treatment of the precipitating cause. i.e. acute
gastroenteritis is of paramount importance for maintenance of normal renal
perfusion.
Discussion:
1. Intravascular volume replacement:
- Balanced crystalloids (i.e. Lactated Ringer’s) has been shown to be more
physiological and superior to isotonic sodium chloride in clinical trials
[namely Saline Against Lactated Ringer’s in Emergency Department trial
(SALTED trial)]
- So, RL should be preferred over NS for volume replacement purpose
- Monitoring of urine output by maintaining a strict intake-output chart is
important to prevent complications arising from hypervolemia from
overzealous IV fluid administration (pulmonary edema) and hypovolemia
(hypotension and circulatory shock)
- Restoration of normal renal perfusion is usually followed by normalization
of serum creatinine level. However, a persistently high serum creatinine
level even after adequate intravascular volume replacement should be
actively investigated for exclusion of underlying chronic kidney disease [by
USG-KUB, which shows altered bilateral renal corticomedullary
differentiation and/or shrunken kidneys in CKD].
2. Treating electrolyte imbalances:
- Hyponatremia: Restriction of oral intake of free water with cautious ORS/
IV fluid (RL>NS) administration in case of mild/ moderate hyponatremia
arising from AGE and hypertonic saline (3% NaCl) in case of severe/
symptomatic hyponatremia
- Hypokalemia: Oral potassium chloride syrups or IV KCl infusion (20-40
mEq in 250/500 ml NS slow IV over 12 hours; followed by rechecking of
serum K+ level)
- Hypomagnesemia: IV Magnesium sulfate (2 gm in 100 ml NS over 2 hours)
- Hypochloridemia: Usually corrected by IV fluid itself
- Metabolic acidosis: Restriction of dietary protein and IV Sodium
bicarbonate if necessary (HCO3 <15 mEq/L).
3. Treatment of underlying cause (acute gastroenteritis):
- Control of dehydration: Oral rehydration solution [ORS]/ IV fluids (RL>NS)
- Control of diarrhea: by oral Zinc supplementation/ oral Loperamide/ oral
Racecadotril
 - Routine administration of antibiotics in all cases of acute gastroenteritis is
not recommended but they should be considered in case of dysentery and in
patients with persistent high-grade fever suggestive of GI sepsis.

What is CRF? Enumerate different causes. Discuss briefly clinical features and
management in a case of CRF. [2+2+3+3]
Chronic renal failure:
Chronic renal failure/ Chronic kidney disease (CKD) is a collective term covering
all primary disease processes that result in structural or functional kidney
abnormalities, or both, persisting for at least 3 months.
Causes of CKD:
The most common primary diseases causing CKD and ultimately end-stage renal
disease (ESRD) are as follows:
1. Diabetic nephropathy
2. Hypertension
3. Primary glomerulonephritis
4. Secondary glomerulonephritis or vasculitis
5. Chronic Tubulointerstitial nephritis
6. Hereditary or cystic diseases
7. Plasma cell dyscrasias or neoplasm
8. Sickle Cell Nephropathy.

Clinical features of CKD:

Clinical features Mechanism & important points
Volume overload Impairment in the tubular excretion of sodium and
(Peripheral edema) water  Extracellular fluid volume expansion
Hyperkalemia Impairment of urinary potassium excretion in the distal
nephron; aggravated by concomitant use of RAS
inhibitors & potassium sparing diuretics (i.e.
Spironolactone)
Metabolic acidosis Failure to excrete adequate H+ to maintain acid-base
balance in the body
 Anemia of chronic 1. Decreased synthesis of Erythropoietin from renal
disease cortex (Most important mechanism)
2. Uremia  Anorexia  Nutritional deficiency of
iron/ folate/ vitamin-B12
3. Uremia  Erosive gastritis  Occult GI blood
loss.
Bone manifestations of 1. Defective 1α-hydroxylation of vitamin D in
CKD kidney  Deficiency of active vitamin D3 
Defect in bone mineralization  Osteomalacia
2. Uremia  ↑↑PO4 level  ↓↓Serum calcium 
Secondary hyperparathyroidism  ↑Osteoclast
activity  Bone resorption  Osteitis cystica
fibrosa  Hemorrhagic bone cyst  Brown
tumor
3. Uremia  ↓Osteoblast activity  Poor weight
bearing  Defective bone remodelling 
Adynamic bone disease  Increased incidence
of bone pain and fracture.
Heart failure 1. Uremia  Increased permeability of alveolar
capillary membranes  Pulmonary edema
2. Anemia/ placement of an AV fistula for
hemodialysis  High cardiac output state 
High-output heart failure.
Increased tendency to 1. Decreased activity of platelet factor III
bleeding and bruising 2. Abnormal platelet aggregation and adhesiveness.
Neurological 1. Early stage CKD: Mild disturbances in memory
manifestations of CKD and disturbances in concentration and sleep
2. Late stage CKD: Hiccups, cramps, twitching;
peripheral neuropathy, Restless leg syndrome
3. Advanced untreated CKD: Asterixis, myoclonus,
seizures, and coma.
GI manifestations of Uremia  Inflammation of gastric mucosa  Erosive
CKD gastritis, peptic ulcer disease, and mucosal ulcerations
 Abdominal pain, nausea, vomiting, anorexia and
occult GI bleeding.
Complications of CKD 1. Hypertension and left ventricular hypertrophy:
Most common complications of CKD
2. Uremic pericarditis [sometimes progressing to
pericardial effusion]:
 ▪ Patient presents with chest pain and shortness
of breath
▪ Characterized clinically by a pericardial
friction rub
▪ ECG shows PR segment depression and
diffuse ST segment elevation
▪ Indication to start the patient on dialysis.
3. Uremic encephalopathy:
▪ Seen when eGFR stays below 15 ml/min for a
prolonged duration
▪ Cognitive dysfunction, drowsiness,
disorientation, confusion, and coma
▪ Indication to start the patient on dialysis.

Management of CKD:
Manifestation Management
Volume overload • Fluid restriction
• Dietary salt restriction
• Use of loop diuretics (Furosemide/ Torsemide)
± Use of Metolazone.
Hyperkalemia • Avoidance of potassium sparing diuretics
• Dose reduction of ACE inhibitors/ ARB
• Potassium binding resins
• Emergency management of severe
hyperkalemia (K+ ≥6.5 mmol/L):
1. IV (Insulin + Dextrose)
2. Levosalbutamol nebulization
3. IV Calcium gluconate.
• Intractable hyperkalemia is an indication to
start the patient on dialysis.
Metabolic acidosis • Oral sodium bicarbonate (500 mg TDS)
• Recent studies suggest that this replacement
should be considered when serum bicarbonate
concentration falls below 20–23 mmol/L to
avoid the protein catabolic state seen with even
mild degrees of metabolic acidosis and to slow
the progression of CKD.
 Hyperphosphatemia • Oral phosphate binders: Calcium acetate/
calcium carbonate
• Sevelamer (400 mg BD-TDS): Non-calcium
containing polymer; does not predispose CKD
patients to hypercalcemia.
Bone disorder in CKD • Oral vitamin D3 supplementation
• Cinacalcet (30 mg OD): Used to treat
secondary hyperparathyroidism in patients with
CKD. Cinacalcet reduces circulating PTH
levels by increasing the sensitivity of the
Calcium sensing receptor (CaSR) to
extracellular calcium.
Hypertension • ACE inhibitors/ ARB: Slow the rate of decline
of kidney function by reduction of the
intraglomerular hyperfiltration and
hypertension. Risk of hyperkalemia and AKI
should be taken into account; in case of
progressive decline in eGFR, these agents
should be discontinued.
• The KDIGO guidelines recommend treatment
with an ACE inhibitor or ARB in all adults with
diabetes and a urinary albumin excretion
exceeding 30 mg/day
• Often the concomitant use of Furosemide with
Metolazone can improve potassium excretion
in addition to improving blood pressure
control.
Anemia • Iron supplementation to replenish iron store
(after doing an iron profile)
• Vitamin B12 and folate supplementation (after
checking blood levels if possible)
• Erythropoiesis stimulating agents (ESA):
1. Erythropoietin
2. Darbepoetin.
• Current practice is to target a hemoglobin
concentration of 10–11.5 gm/dL.
Abnormal hemostasis • Abnormal bleeding time and coagulopathy in
CKD patients may be reversed temporarily
 with desmopressin, cryo-precipitate, blood
transfusions, and ESA therapy
• Optimal dialysis will usually correct a
prolonged bleeding time.

Short note: Renal replacement therapy [RRT]. [5]

Introduction:
Renal replacement therapy (RRT) is a term for treatments that replace the
metabolic waste filtering functions of a normal kidney. RRT techniques include:
1. Intermittent hemodialysis
2. Continuous hemofiltration and hemodialysis
3. Peritoneal dialysis:
a. Continuous ambulatory peritoneal dialysis (CAPD)
b. Continuous cyclic peritoneal dialysis (CCPD)
4. Renal transplantation.
Indications to start a patient on RRT:
✓ Anorexia and nausea not attributable to reversible causes (Ex: PUD)
✓ Evidence of malnutrition
✓ Refractory hyperkalemia unresponsive to conservative measures
✓ Refractory extracellular fluid volume overload despite diuretic therapy
✓ Uremic encephalopathy
✓ Uremic pericarditis.
Brief overview of hemodialysis filter (Dialyzer):